Microplastics

The Summary

Links Between Microplastics and Diabetes/Obesity

There is not a lot research (yet) on micro or nanoplastics or nanomaterials and diabetes or obesity, but the research field is beginning to grow.

The Details

Reviews on Microplastics and Diabetes/Obesity

A review finds that laboratory animals exposed to microplastics and their additives develop inflammation, immunological responses, endocrine disruption, and alterations in energy metabolism; microplastics are potential obesogens, and could promote non-alcoholic fatty liver disease (NAFLD) by modifying gut microbiota composition (Auguet et al. 2022). A review finds that both nano- and micro-plastics can disturb the gut microbiota and intestinal barrier, and affect the immune system (Hirt and Body-Malapel 2020). (Changes to the gut microbiota and gut barrier are linked to type 1 diabetes; see the Diet and the Gut page).

Human Studies on Microplastics and Diabetes/Obesity

There are not many studies yet on microplastics in humans. One, however, did find that microplastics may affect the gut microbiota in Chinese preschoolers (Ke et al. 2023). There aren't any studies on microplastics and diabetes or obesity yet, in humans.

Laboratory Studies on Microplastics and Diabetes/Obesity

Zebrafish exposed to polyethylene microplastics had significant changes in microbiome, changed levels of triglycerides, total cholesterol, fatty acids, and glucose, and lowered transcription levels of glucose and lipid metabolism-related genes (Zhao et al. 2021).

In mice, combined exposure to lead and microplastics (PVC and polyethylene) caused insulin resistance and impaired glucose tolerance (Zhu et al. 2024).

In mice, nanoplastic exposure via mother mice led to increased body weight in offspring during "childhood," linked to gut microbiota changes (Jeong et al. 2024).

In beta cells in vitro and in mice in vivo, microplastics and phthalates combined synergistically to cause beta cell death and oxidative stress (Wang et al. 2022). 

Test tube screening of microplastic extracts from Italian waters showed potential effects on metabolism, including increased fat cell development and fat uptake and storage (Capriotti et al. 2020).

Acute exposure to microplastics at environmentally relevant concentrations disrupted gut microbiota and metabolism in zebrafish (Medriano and Bae, 2022).  Exposed to the same amount of microplastics, zebrafish that ate a high-fat diet had higher levels of microplastics in their tissues than those that ate a normal diet. Microplastics exacerbated liver injury in combination with a high-fat diet (Du et al. 2023). 

In mice, microplastics caused higher blood glucose levels and glucose intolerance (despite decreased body weight) and fatty liver (Li et al. 2024).

Polystyrene micro and nanoplastics

Exposure to polystyrene microplastics at levels relevant for human exposure caused intestinal inflammation, insulin resistance, high blood glucose levels, and diabetes in mice (Shi et al. 2022). Mice fed polystyrene microplastics developed insulin resistance on both a high-fat and normal diet, plus inflammation and changes to the gut microbiome (Huang et al. 2022). Also in mice, polystyrene microplastic exposure promoted fat cell differentiation and interfered with muscle cells (Shengchen et al. 2021). Polystyrene nanoplastics also have effects on cells that could contribute to fat build up and heart disease (Florance et al. 2021). In mice, polystyrene microplastics caused metabolic disorders in the mothers, along with changes in the gut microbiota and gut barrier dysfunction, as well as long-term metabolic consequences in the first and second generation offspring (Luo et al. 2019a), including affecting cholesterol and triglyceride levels (Luo et al. 2019b). In mice, polystyrene nanoplastics caused high glucose levels, increased cholesterol and triglyceride levels, increased insulin resistance, oxidative stress, and organ injury (Fan et al. 2021).  ​Polystyrene microplastics increased gut inflammation, blood glucose, lipid (cholesterol/triglyceride) levels, and signs of non-alcoholic fatty liver disease (NAFLD), but only in mice fed a high-fat diet (Okamura et al. 2023).  Mice exposed to high levels of microplastics lost weight, while those at somewhat lower levels became overweight (Huang et al. 2023). 

In rats, polystyrene microplastics caused glucose intolerance and higher insulin, triglyceride, and LDL cholesterol levels, and lower HDL cholesterol levels (Saeed et al. 2023). Mice who ate polystyrene microplastics gained weight and fatty tissue, and but not fatty liver disease. The effects were reduced by an compound found in berries (Zhao et al. 2024). 

Zebrafish exposed to polystyrene microplastics and an antibiotic had higher levels of triglycerides and cholesterol, as well as inflammation and oxidative stress in their livers, and changes to the gut microbiome and intestinal injury (Zhou et al. 2023). 

In mice fed a high-fat diet, polystyrene nanoplastics accumulated in beige fat tissue and suppressed energy expenditure, increased fat mass, insulin resistance and fatty liver, and disrupted glucose control. The effects were lessened by antioxidants (Zhang et al. 2024).

In mice, exposure to polystyrene nanoplastics caused liver fat accumulation; the effects ended 50 days after exposure stopped (Lu et al. 2024). 

Mice with diabetes were more susceptible to the health effects of polystyrene microplastics than mice without diabetes (Liu et al. 2022). 

Polystyrene nanoparticles caused insulin resistance in mice (Fan et al. 2024). Also in mice, polystyrene nanoplastics caused larger fat cell size, induced intestinal inflammation, and increased fat accumulation in the liver (Shiu et al. 2022). These materials also affected glucose levels in crabs (Nan et al. 2022). In pregnant mice, maternal exposure to polystyrene nanoplastics caused fetal growth restriction and disturbed cholesterol metabolism in both the placenta and fetus (Chen et al. 2022).  In mice, exposure to polystyrene nanoplastics alone induced an increase in blood glucose, glucose intolerance and insulin resistance, while combining that with a high-fat diet and streptozocin (a chemical that kills beta cells) made it all worse (Wang et al. 2023). Polystyrene micro and nano-plastics at levels found in the environment increased body weight and affected gut microbiota in silkworms (Muhammad et al. 2023). In mice, polystyrene micro and nano plastics (at levels we are exposed to) caused changes to the gut microbiota, intestinal inflammation, intestinal barrier malfunction, and immune system changes (Zhang et al. 2023). Polystyrene microplastics also affect the liver and lipid levels (Tao et al. 2024).

Polystyrene nanoplastics increased fasting blood glucose levels, glucose intolerance, and insulin resistance in mice (Wang et al. 2024). 

Polystyrene nanoparticles enhanced the toxicity of high glucose in roundworms (Zhuang et al. 2024).  

Mice exposed to airborne nanoplastics developed insulin resistance, glucose intolerance, and high blood glucose (Yang et al. 2024). 

Exposure to microplastics and triclosan disrupted lipid metabolism in zebrafish; the effects of unaged microplastics were worse than aged (Liu et al. 2024). 

Nanomaterials

A review finds that nanoplastics can enter the gut and disturb the gut microbiome, and have heath effects related to diabetes and obesity (Haldar et al. 2023). 

Exposure to nanomaterials/nanoparticles may be linked to diabetes development (Ali 2019; Guo et al. 2019; Mao et al. 2019;  Mohammadparast and Mallard, 2022; Priyam et al. 2018). Titanium dioxide nanoparticles, for example, have been widely used in numerous applications and caused pancreatic tissue damage, including in islets, which became worse with increased duration of exposure. Decreased immune expression of the insulin protein together with decreased serum insulin and increased blood glucose levels indicated the alteration of beta cells by titanium dioxide nanoparticles (Abdel Aal et al. 2020).  In mice with gestational diabetes, exposure to titanium dioxide nanoparticles increased blood glucose levels and had other negative effects on the fetuses (Chen et al. 2021). These particles may also affect the gut microbiota and contribute to obesity (reviewed by Lamas et al. 2023).

In mice, perinatal exposure to silver nanoparticles through the mother led to chronic inflammation in offspring which persisted until adulthood, pancreatic damage, reduced insulin levels, increased blood glucose levels, and kidney damage (Tiwari et al. 2021). 

Long-term oral exposure to dietary nanoparticles at doses relevant for humans disrupts gut microbiota composition and function in mice, but did not cause glucose intolerance or other disease effects (Perez et al. 2021). In mice, nanoplastics increase gut barrier permeability and inflammation (Kim et al. 2024). 

Exposure During Development

An interesting study of the effects of polyethylene microplastics in an invertebrate found that in the parents, the exposure had opposite effects depending on dose (low dose stimulation and high dose inhibition). In the offspring, increasing exposures increased the effects. In the subsequent, unexposed generation there were no effects (Lu et al. 2024). 

Polystyrene micro/nanoplastics affected development and lipid metabolism in zebrafish embryos (Xin et al. 2024).